GC209 Urinary Incontinence And Overactive Bladder
Urinary incontinence is the involuntary loss of urine, while overactive bladder is a syndrome characterized by urgency, with or without urge incontinence, usually accompanied by frequency and nocturia, resulting from detrusor muscle overactivity or other lower urinary tract dysfunction.
Urinary Incontinence and Overactive Bladder
Big Idea: Urinary incontinence (UI) and overactive bladder (OAB) are extremely common conditions that arise from a failure of the normal storage/voiding interplay between the bladder (detrusor) and the sphincteric mechanism. Understanding the physiology of micturition is the key to understanding why each type of incontinence occurs and how each treatment works. This lecture covers first principles of neuroanatomy and bladder physiology, then builds toward classification, clinical assessment, urodynamics, and a structured treatment ladder — from conservative measures all the way to urinary diversion.
Learning Objectives [1]:
- Physiology of micturition
- Aetiology, pathophysiology and prevalence of urinary incontinence
- Aetiology, pathophysiology and prevalence of overactive bladder
- Role of urodynamic study in urinary incontinence and overactive bladder
- Treatment of urinary incontinence and overactive bladder
How it fits: This lecture connects to BPH/BOO (GC 180), paediatric urology/enuresis (GC 213), female pelvic floor/prolapse (GC 116), spinal cord injury (GC 110), geriatric medicine (GC 037), and diabetic complications (GC 042). Examiners love testing the DIAPERS mnemonic, the drug causes table, the difference between stress and urge incontinence, antimuscarinic side effects, and the OAB treatment ladder.
1. Physiology of Micturition
The bladder has dual innervation (somatic, autonomic) with higher centre modulation. Get this right and every pathology makes sense. [1]
| Nerve | Origin | Receptor/Target | Function |
|---|---|---|---|
| Pudendal nerve (somatic) | S2–S4, Onuf's nucleus (anterior horn) | Nicotinic receptors on striated muscle | External urethral sphincter, anterior levators, superficial perineal muscles — voluntary continence |
| Pelvic nerve (parasympathetic) | S2–S4 | Muscarinic (M3 > M2) on detrusor | Detrusor contraction, bladder neck relaxation, levator ani — voiding |
| Hypogastric nerve (sympathetic) | T10–L2 | β₃-adrenergic on detrusor body; α₁-adrenergic on bladder neck/urethra | Detrusor relaxation (β₃) + bladder neck contraction (α₁) — storage |
The hypogastric nerve forms the pelvic plexus with the parasympathetics [1]
Why this matters: During storage, sympathetic tone keeps the detrusor relaxed (β₃) and the bladder neck closed (α₁), while the pudendal nerve keeps the external sphincter tonically contracted. During voiding, parasympathetic activation contracts the detrusor (M3), while somatic and sympathetic tone are inhibited — the sphincter relaxes. If you understand this, you understand why β₃-agonists (mirabegron) help OAB, why antimuscarinics reduce detrusor contractions, and why α-blockers can worsen stress incontinence.
Higher centres [1]:
- Pontine micturition centre (PMC): The actual organizational centre for the micturition reflex. Receives afferent stretch input from detrusor and cerebellar input for coordinated voiding.
- Frontal cortex: Provides inhibitory input to PMC — this is why frontal lobe lesions (e.g., dementia, NPH, frontal tumours) cause urge incontinence.
- Sacral micturition centre: Communicates with pons to execute the micturition reflex arc.
- Cerebellum: Coordinates smooth voiding.
What the physiology diagram shows (FILLING): brain → lateral pontine continence centre; sympathetic T10–L2 relaxes detrusor / closes internal sphincter; Onuf’s nucleus (S2–S4) keeps external sphincter closed — until ~400 mL stretch flips the circuit toward the medial pontine micturition centre. [1]
Key Concept: Suprasacral vs Sacral Lesions
Suprasacral spinal cord injury: Acutely → spinal shock → areflexic bladder → retention/overflow. Later → loss of cortical inhibition → detrusor overactivity (urge incontinence) ± detrusor-sphincter dyssynergia (DSD).
Sacral cord / cauda equina injury: Loss of parasympathetic drive → areflexic/hypotonic bladder → overflow incontinence (this pattern is permanent, not biphasic like suprasacral).
"A reflex action at the level of spinal cord with stimulation by full bladder with sudden complete relaxation of sphincter muscles and immediately followed by detrusor contraction. Organized in pontine micturition centre. Voluntary control at cortical level." [1]
Sequence:
-
Bladder fills → afferent stretch fibres (Aδ fibres) via pelvic nerve → sacral cord → pons
-
PMC integrates cortical permission + cerebellar coordination
-
Efferent parasympathetic → detrusor contracts
-
Simultaneous somatic inhibition → external sphincter relaxes
-
Voiding occurs at low pressure with coordinated flow
~400 mL of bladder filling excites the micturition reflex [1]
Additional voiding physiology points [1]:
- The brainstem (PMC) is the actual organizational centre for the micturition reflex in an intact neural axis
- Intravesical pressure initiates micturition for involuntary induced emptying
- Voluntary emptying involves inhibition of somatic neural efferent activities
- Sympathetic inhibition → bladder neck opens
2. Bladder Function: Storage and Voiding
Storage (filling): Efficient and low-pressure filling, lower pressure storage and perfect continence [1]
Voiding: Periodic voluntary urine expulsion at low pressure [1]
- Accommodation of urine at low pressure — the bladder is highly compliant (elastic walls)
- Bladder outlet closed at rest and during rises in intra-abdominal pressure
- No involuntary detrusor contractions during filling
- Coordinated detrusor contraction of adequate magnitude
- Concomitant lowering of resistance at the sphincter level
- No anatomical obstruction
Compliance = ΔV / ΔPdet (expressed as mL per cm H₂O) [1]
Normal compliance: large volume change with little increase in pressure [1]
Decreased compliance: small change in volume resulting in large increase in pressure [1]
Why compliance matters: A poorly compliant bladder generates high pressures during filling → transmits back-pressure to ureters → obstructive uropathy and renal damage. Think of it as: "How thick, how big and how elastic is this bladder" [1].
Causes of decreased compliance [1]:
- Processes that alter viscoelasticity of the wall (fibrosis, radiation, chronic inflammation)
- Filling beyond limits of distensibility
- Filling at a rate exceeding stress relaxation rate
- Neurological and structural disease (SCI, interstitial cystitis, radiation cystitis, post-hysterectomy)
Ketamine cystitis: Chronic ketamine abuse → small low-compliance bladder → urge incontinence and frequency. Ureteric obstruction can cause obstructive uropathy. [1]
Continence depends on: normal CNS, spinal cord control, anatomically normal lower urinary tract [1]
Three pillars of continence [1]:
- Anatomical support by intact pelvic floor — holds bladder neck and urethra in place (especially important in females)
- Intrinsic urethral mechanism: Coaptation of mucosa, compression by submucosa, and by internal/external sphincters
- In males, the prostate acts as part of the continence device — hence post-prostatectomy incontinence
Why Females Are More Susceptible to SUI
Women lack a prostate. Their continence relies heavily on pelvic floor muscular support and the intrinsic urethral mechanism. Childbirth, menopause (oestrogen withdrawal → mucosal atrophy), and pelvic surgery weaken these supports → stress incontinence.
"Any type of voiding dysfunction or continence problem must result from an abnormality of one or more of the factors mentioned including structural abnormalities of various causes" [1]
This is best understood as an interaction between bladder and sphincter:
| Component | Storage Failure | Voiding Failure |
|---|---|---|
| Bladder | Detrusor overactivity (idiopathic, neurogenic) or low compliance → urge incontinence | Detrusor underactivity (DUA) → retention/overflow |
| Sphincter | Extrinsic: Urethral hypermobility (weak pelvic floor) → stress incontinence; Intrinsic: ISD (↓urethral musculature, blood flow, innervation) → severe stress incontinence | Sphincter dyssynergia (failure to relax during voiding) → retention |
Definition (ICS): "Condition where involuntary loss of urine is a social or hygienic problem and is objectively demonstrable" [1]
Severity ranges from dribbling small amounts of urine to continuous urinary incontinence [1]
Prevalence [1]
| Population | Prevalence |
|---|---|
| Premenopausal women | 25% |
| Women > 65 years | 40% |
| Men > 65 years | 15% |
| F >> M overall | Peak age 50–70 |
Of all UI [1]:
- Stress incontinence: 50%
- Urge incontinence: 11%
- Mixed incontinence: 36%
50–75% of patients NEVER complain to physicians [1] 80% of urinary incontinence can be cured or improved [1]
This is the single most tested classification in this lecture.
| Type | Definition [1] | Mechanism | Key Features |
|---|---|---|---|
| Stress UI (SUI) | Urine leakage on effort, exertion, sneezing or coughing | Occurs when bladder pressure exceeds urethral pressure under increased abdominal pressure | Caused by sphincter weakness: urethral hypermobility ± ISD (F), post-prostatectomy (M) |
| Urge UI (UUI) | Leakage accompanied by or immediately preceded by urgency (sudden strong desire to void) | Uncontrolled detrusor contraction overcomes urethral resistance | "OAB," can be worsened by stress/anxiety, often mixed with SUI |
| Mixed UI | Leakage with urgency AND with effort/exertion/sneezing/coughing | Both mechanisms | Treatment should focus on predominant symptom |
| Overflow incontinence | Leakage when bladder abnormally distended with large residual volume | Overdistension of bladder: obstructive (BPH) or hypotonic detrusor (meds, SCI, diabetic cystopathy) | Frequent/constant "dribbling," significant PVR, palpable bladder |
| Functional incontinence | Leaking due to inability to get to toilet | Cognitive/physical/environmental limitations | Diagnosis of exclusion — elderly, impaired mobility, dementia |
Overflow Incontinence Complications
Chronic retention with overflow may be complicated by UTI, bladder stone formation, and eventually obstructive uropathy with deterioration of renal function. [1] — This is commonly asked: always check RFT in patients with chronic retention!
6.1 Enuresis [1]
Enuresis: any involuntary loss of urine. Nocturnal enuresis = involuntary loss during sleep. In paediatric population: up to 10–12% at 5 years old. Most improve with age.
7. Aetiology and Risk Factors
| Category | Risk Factors |
|---|---|
| Unmodifiable | White race, age (especially menopause ~50), female sex |
| Modifiable | Smoking, caffeine, obesity, poor mobility, fluid intake |
| Diseases/conditions | Vaginal childbirth, UTI, DM, neurological disease (CVA, Parkinsonism, MS, SCI), anatomical disorders (VVF, ectopic ureter, urethral diverticulum), pelvic/perineal/prostate surgery, radiotherapy, medications |
- Congenital: Duplex ureter with insertion below external sphincter (continuous incontinence in a girl since birth!)
- Infection
- Iatrogenic: Post-prostatectomy sphincteric injury
- Birth injury: Vesicovaginal fistula, stress incontinence
- Neoplastic
| Category | Causes |
|---|---|
| Idiopathic DO | Most common |
| Non-neurogenic DO (secondary to bladder pathology) | BOO (BPH, urethral stricture), bladder stone/FB, bladder tumour (CIS!), infection/inflammation (cystitis) |
| Neurogenic DO | CVA, Parkinson's disease, brain tumour, TBI, MS; Spinal cord lesions (injury, tumour, transverse myelitis, myelodysplasia) |
This mnemonic is high yield for both MCQ and SAQ.
| Letter | Cause | Why it causes incontinence |
|---|---|---|
| D | Delirium | Altered sensorium → cannot perceive/respond to urge |
| I | Infection | Cystitis irritates detrusor → urgency/urge incontinence |
| A | Atrophic vaginitis/urethritis | Post-menopausal oestrogen loss → mucosal thinning → reduced urethral coaptation |
| P | Pharmaceuticals | See drug table below |
| P | Psychological disorders | Depression, anxiety |
| E | Endocrine disorders | DM (polyuria, cystopathy), hypercalcaemia, DI |
| R | Restricted mobility | Cannot reach toilet → functional incontinence |
| S | Stool impaction | Rectal distension → mechanical pressure on bladder/urethra → retention/overflow |
| Drug/Substance | Type of Incontinence Caused | Mechanism |
|---|---|---|
| Diuretics | Urge | ↑Urine production → bladder overdistension → urgency |
| Caffeine | Urge | Irritant to detrusor + mild diuretic |
| Alcohol | Urge | Diuretic + CNS sedation |
| Anticholinergics | Overflow | ↓Detrusor contractility → retention |
| Alpha agonists | Overflow | ↑Urethral resistance → outflow obstruction |
| Beta agonists | Overflow | Detrusor relaxation (β₃) → retention |
| Sedatives / Antidepressants | Overflow | ↓Detrusor contractility + sedation |
| ACE inhibitors | Stress | Chronic cough → ↑intra-abdominal pressure |
8. Clinical Approach to UI
Duration, type (stress/urge/mixed), triggers, obstructive symptoms, pad usage (number/size/wetness), lifestyle (caffeine/smoking/alcohol), menstrual/obstetric history, bowel symptoms, previous pelvic surgery/diabetes, drugs.
- Voiding diary (24–72 hours): fluid intake, physical activity, frequency, void volume, incontinence episodes and triggers [1]
- Estimates: 24h urine volume, voiding frequency, nocturia, functional bladder capacity
"Above the waist":
- Abdominal exam: Palpable bladder? Masses?
- General neurological examination
Genital exam:
- Atrophy, cystocele, rectocele, pelvic masses, skin excoriations
PR examination:
- Anal tone ± faecal soiling, prostate (M), faecal impaction, rectal mass
- Reflexes: Anal reflex, cough reflex, bulbocavernosus reflex (BCR) — S2,3,4
- Look for: Parkinson's disease, MS, CVA signs; sensory/motor/reflex abnormalities
| Investigation | Details |
|---|---|
| Frequency/volume chart (voiding diary) | Semi-objective symptom quantification |
| Uroflowmetry + residual volume | Normal RU < 50 mL (by uroflow); < 150 mL by other references |
| Urinalysis ± culture | Rule out UTI |
| Renal function | Rule out obstructive uropathy |
| Fasting glucose | Rule out DM (diabetic cystopathy, polyuria) |
| Urodynamic study | Gold standard, only for complex cases |
Goals:
- Duplicate patient's symptoms
- Determine aetiology of incontinence
- Evaluate detrusor function
- Determine degree of pelvic floor prolapse
- Identify urodynamic risk factors for upper tract deterioration
Indications for UDS [1]:
- Clinical suspicion of detrusor overactivity
- Voiding dysfunction
- Unclear clinical diagnosis before surgery
- Previous surgery for stress incontinence
- Presence of neurological clinical features
Components of UDS [1]:
- Flowmetry: Flow rate and residual urine
- Filling phase: Instability (DO) or hypotonia (DUA)
- Voiding phase: Obstruction
- Video-UDS: Better evaluation of bladder neck descent, urethra, anterior wall prolapse
- EMG: Striated sphincter activity
- LPP (Leak Point Pressure), UPP (Urethral Pressure Profile)
Video-UDS advantage: Better evaluation of bladder neck descent & urethra; more accurate quantification of anterior wall prolapse [1]
Clinical vs Urodynamic Diagnosis
From GC 116 [3]: Stress UI is a clinical diagnosis (leakage on effort/cough). Urodynamic stress incontinence = leakage during filling cystometry with ↑abdominal pressure and NO detrusor contraction. OAB is a clinical diagnosis; detrusor overactivity = involuntary detrusor contractions on filling cystometry. These are distinct terms and examiners may test the difference.
9. Treatment of Urinary Incontinence
"Treat according to the cause" [1]
9.1 Treatment Ladder for OAB [1]
Lifestyle modification:
- Fluid management, decrease caffeinated drinks (improves frequency and urgency but NOT UI)
- Stop smoking (weak evidence)
- Weight loss: PRIDE study, BMI > 25 → 40% reduction in urgency incontinence episodes with mean weight loss of 8% at 6 months
Bladder re-training (6 months):
Principles: Central control of voiding can be relearned as in infancy [1]
- Timed voiding: Urinate on schedule, not in response to urge
- Diversion techniques: Deep breathing, mental calculation, pelvic floor squeezing during urge
- Aim: Decrease urgency and frequency to 2–3 hourly intervals
Pelvic floor muscle training (PFMT / Kegel exercises):
At least 3 months, 60% success [1]
- 15 near-maximal contractions, 10 seconds each with equivalent rest, 3 cycles/day, 30–50 daily contractions
- Rationale: Strengthen pelvic floor musculature → ↑urethral support, regain unconscious pelvic floor activation during ↑abdominal pressure
Oestrogen therapy:
Oral oestrogen INCREASES risk of both stress and urgency incontinence! [1] Vaginal oestrogen therapy in post-menopausal women may improve or cure UUI (Level 1a) [1]
Antimuscarinic drugs [1]:
Muscarinic receptors in bladder: 80% M2, 20% M3. Bladder contractions involve M3. [1]
MOA: Competitive antagonist at post-synaptic M3 → inhibits phospholipase C/IP3 pathway → ↓Ca²⁺ channel opening → ↓intracellular calcium → reduced smooth muscle contraction [1]
- Take 3–4 weeks to work
- NICE: tried at least 2 types before considered failure
| Drug | Special Features |
|---|---|
| Oxybutynin | Available as ER, transdermal, intravesical, rectal forms. ER/transdermal avoid first-pass → less desethyloxybutynin (major cause of S/E) |
| Tolterodine | Functional selectivity for bladder over salivary gland → less dry mouth |
| Solifenacin | Selective M2 and M3; no cognitive dysfunction in elderly (Level 1b) |
| Darifenacin | Selective M3; no cognitive dysfunction in elderly |
| Trospium chloride | Quaternary amine → less lipophilic → does NOT cross BBB → less CNS side effects |
| Propantheline | Quaternary amine |
| Fesoterodine | No cognitive dysfunction in elderly (Level 1b) |
Side effects by receptor:
- M1: Cognitive impairment (important in elderly!)
- M2: Tachycardia, constipation
- M3: Dry mouth (25%), constipation (4%), blurred vision, dizziness
Contraindications [1]:
- Uncontrolled acute closed-angle glaucoma
- Ulcerative colitis / toxic megacolon
- Myasthenia gravis
- Intestinal obstruction
Efficacy [1]:
Meta-analysis (Chapple): ↓frequency by 1/day, ↓urgency by 1/day, ↓incontinence by 1/day, functional bladder capacity ↑10–50 mL. Efficacy 70%. [1]
No consistent evidence that one antimuscarinic is superior to another (Level 1a) [1]
> 50% of patients stop antimuscarinics within first 3 months due to ineffectiveness, adverse events, costs [1]
Options if dry mouth intolerable [1]:
- Switch to ER formulation
- Switch to tolterodine (functionally selective)
- Switch to mirabegron
- Transdermal/intravesical oxybutynin (but high withdrawal due to skin reaction)
Beta-3 agonists — Mirabegron [1]:
MOA: Activates adenylyl cyclase → ATP to cAMP → protein kinase A → ↓intracellular calcium → smooth muscle relaxation [1]
- Dose: 25 mg/50 mg daily (up to 100 mg)
- Side effects: Hypertension, headache, UTI, nasopharyngitis
- DH warning: severe hypertension, CVA, cardiovascular disease reported [1]
- Evidence: Nitti Phase III RCT 2013 → ↓incontinence episodes by 1.5/24h, ↓micturition by 1.6/24h vs placebo
Combination therapy (antimuscarinic + β₃-agonist) [1]:
Possible because they act on different pathways: phospholipase C vs cAMP [1]
- Symphony trial (Abrams 2015): Solifenacin + mirabegron → improved mean voided volume (~20 mL), ↓frequency (~1/day), ↓urgency (~1/day) vs solifenacin monotherapy; slightly higher constipation
- Capsaicin (from hot chili pepper) and resiniferatoxin (RTX) (from African plant, 1000× more potent)
- Target vanilloid receptors on unmyelinated C-fibres of bladder
- More effective in neurogenic DO (NDO)
- Duration ~3 months/dose; requires GA; not readily available
Neurotoxin from Clostridium botulinum; OnabotulinumtoxinA (Allergan) [1]
MOA [1]:
Heavy chain binds SV2 receptor → endocytosed → light chain cleaves SNAP-25 on SNARE complex → blocks ACh exocytosis → detrusor paralysis
Also reduces vanilloid receptor TRPV1 and purinoreceptor P2X3 on C-fibres → ↓urgency [1]
Dosing [1]:
- IDO (idiopathic DO): 100U in 10 mL NS, 20 injection sites (FDA approved)
- NDO (neurogenic DO): 200U in 20 mL NS, 20 injection sites (FDA approved)
- Trigone-sparing to avoid vesicoureteric reflux
- Onset 1–2 weeks; repeat every 6–9 months (neural regeneration; equally effective as first injection)
- Do not shake — breaks disulfide bond
Evidence [1]:
- EMBARK (Nitti 2013): ↓incontinence by 2.65 episodes; 23% completely dry
- Chapple meta-analysis (EU 2014):
- NDO: ↓maximal Pdet 40%, ↓incontinence 60%, ↑MCC 70%
- IDO: ↓maximal Pdet 30%, ↓frequency 30%, ↓urgency 40%, ↓incontinence 60%, ↑MCC 60%
- NEJM 2012 RCT: Botox vs antimuscarinics → similar UI reduction; Botox → less dry mouth, more complete resolution but more UTI and transient retention
Complications [1]:
- Retention requiring CISC: up to 10–20%
- UTI 5%, haematuria 2%, rare systemic absorption
Contraindications [1]: Active UTI, bleeding diathesis, myasthenia gravis, pregnancy/breastfeeding, allergy
Posterior Tibial Nerve Stimulation (PTNS):
- Electrical stimuli to sacral micturition centre via S2–4
- Weekly for 30 min × 12 weeks
- OrBIT trial: comparable to tolterodine; for responders, maintenance every 3 weeks
- Effective for UUI women who failed antimuscarinics (Level 2b)
- No more effective than tolterodine (Level 1b)
Sacral Neuromodulation (InterStim) [1]:
- Two-stage procedure: Temporary electrode in S3 foramen; if > 50% improvement on voiding diary → implant permanent pulse generator near PSIS
- Correct placement confirmed by: dorsiflexion of big toe, bellows reflex (anal wink), sensation of pulling in rectum/scrotum/vagina
- 50% long-term cure, 25% improvement, 25% failure
- Battery life: 7 years
- Indications: Intractable OAB, intractable NDO, Fowler's syndrome, interstitial cystitis, underactive bladder, faecal incontinence
- Complications: infection, migration/displacement (5–10%), explantation rate 10%
Coronal cystotomy ("clam" opening), patch with detubularized ileum (25 cm, 15 cm from ICV). 50% cure. [1]
Rationale: Impairs contraction, lowers pressure, increases capacity, decreases amplitude of contraction.
Contraindications [1]: CrCl < 40 mL/min, liver impairment, non-compliance with CISC, short gut syndrome, IBD, prior RT to bowel.
Complications [1]:
| Early | Long-term |
|---|---|
| Bleeding, infection, collection, anastomotic leak, ileus | Mechanical: CISC need, mucus, perforation, spontaneous rupture |
| Metabolic: Hyperchloraemic hypokalaemic metabolic acidosis (NH₄Cl absorbed in exchange for H₂CO₃; acidosis → osteoporosis) | |
| Malabsorption: ↓Fat absorption → Ca²⁺ binds fat (saponification) instead of chelating oxalate → ↑oxalate absorption → CaOx stones; ↓B12 and bile acid → anaemia, gallstones | |
| Malignancy: Adenocarcinoma (nitrosamines); follow-up cystoscopy post-op 10 years onwards |
9.2 Treatment of Stress Incontinence [1]
Non-surgical:
- Lifestyle: Weight reduction, stop smoking, fluid management
- Incontinence pads
- PFMT / bladder retraining
- Medication: Duloxetine (SNRI — ↑urethral sphincter tone via pudendal nerve), oestrogen therapy (vaginal)
Surgical — divided into occlusive and supportive:
| Approach | Procedure |
|---|---|
| Occlusive | Bulking agents (periurethral injection); Artificial urinary sphincter (AUS) |
| Supportive | Suburethral/mid-urethral sling (TVT), pubovaginal sling, retropubic suspension (colposuspension) |
1995: Tension-free vaginal tape (TVT) by Ulmsten. Objective cure rate > 90% at 10-year follow-up. New gold standard for surgical treatment of female SUI. [1]
Mechanism of action [1]:
- Dynamic kinking of urethra with stress
- Reinforce functional pubourethral ligaments
- Reinforce suburethral vaginal hammock
- Prevent hypermobility of bladder neck from opening mid-urethra
Midurethra closing pressure < 20 cm H₂O predicts surgical failure [1]
Indications [1]: Urethral hypermobility, urodynamic SUI; extended indications include complex SUI, obese/elderly, concurrent prolapse, previous failed surgery.
- For ISD: pubovaginal sling is a better option [1]
Contraindications [1]: Urethrovaginal fistula, urethral diverticulum, intraoperative urethral injury, untreated urinary malignancy.
Types of sling [1]:
- Classic (bladder neck): Rectus fascia, fascia lata, synthetic (polypropylene, Dacron, Gore-Tex)
- TVT (1996): Mid-urethral position, tension-free, polypropylene mesh
- SPARC: Similar mid-urethral position
Three components [1]:
- Urethral cuff — placed at bladder neck in females, bulbous urethra in males
- Scrotal/labial control pump
- Reservoir — preperitoneal retropubic space
Indications: Post-radical prostatectomy, neuropathic patient with ISD, perineal/pelvic trauma.
Contraindications [1]: Poor bladder compliance, untreated detrusor overactivity, urethral stricture, poor cognitive function.
Pre-operative workup [1]:
- Video-urodynamics (assess bladder compliance and confirm ISD)
- Flexible cystoscopy to exclude urethral stricture
- Urine culture and sensitivity
Outcomes [1]:
- Deactivation for 6–8 weeks post-implant
- Complete continence 75%, socially dry 90%, long-term continence 60%
- 50% only have original sphincter at 10 years; 30% removed for infection/erosion; 20% late mechanical failure
Complications: Infection, cuff erosion (usually first 6 months), urethral atrophy (40%), persistent leakage, mechanical failure.
Perform UDS in ALL patients before surgery:
- Confirm diagnosis
- Assess bladder contractility and residual urine
- Look for mixed incontinence for better counselling
10% of patients with SI have DO and 20% of patients with DO have SI [1]
10. Integration with Related Material
From GC 110 and Ryan Ho Neurology [7]: Suprasacral lesions → spinal shock (retention/overflow) → later DO ± DSD. Sacral lesions → permanent areflexic bladder → overflow. DSD can cause high-pressure reflux → reflux nephropathy.
From GC 180 and Maksim Surgery Notes [5]: BPH causes BOO → compensatory detrusor hypertrophy → secondary DO (up to 30–60% of BOO patients develop OAB) → if untreated → decompensation → DUA → chronic retention → overflow incontinence. Treatment of BOO (e.g., α-blockers, TURP) may resolve secondary OAB.
From Ryan Ho Endocrine [8]: Autonomic neuropathy → ↓ability to sense full bladder → incomplete emptying → recurrent UTI → overflow incontinence.
From GC 213, Adrian Lui Paeds [9]: Primary monosymptomatic nocturnal enuresis in children ≥ 5 years. Treatment: behavioural (fluid restriction, enuresis alarm — first-line) → desmopressin (↓nocturnal urine output) → anticholinergics if OAB features.
From GC 116 [3]: Pelvic floor includes peritoneum, viscera, endopelvic fascia, levator ani, perineal membrane, superficial genital muscles. Vaginal childbirth, menopause, chronic ↑abdominal pressure → pelvic floor weakness → SUI and pelvic organ prolapse.
Common Traps and Discriminators
| Trap | Why Students Get It Wrong |
|---|---|
| "SUI is worse at night" | No! SUI is worse with activity (cough, sneeze, exertion). If incontinence is worse at night → think overflow or enuresis. |
| Confusing OAB with UTI | Both have urgency/frequency. OAB = sterile urine; UTI = pyuria/bacteriuria. Always send MSU C/ST. |
| Oral oestrogen for UI | Oral oestrogen WORSENS incontinence. Only vaginal oestrogen helps. |
| Antimuscarinics cause retention | True — hence they are contraindicated in untreated BOO. But in OAB they are first-line pharmacotherapy. |
| Urodynamics as first-line Ix | No. First-line = MSU C/ST and voiding diary. UDS is gold standard but reserved for complex/surgical cases. |
| "Mirabegron has no side effects" | It can cause hypertension and cardiovascular events. DH warning highlighted in lecture. |
| IPSS as diagnostic tool | IPSS quantifies severity of LUTS — it is NOT a diagnostic tool. |
| Pressure-flow study vs filling cystometry | Pressure-flow study diagnoses BOO (high Pdet + low flow). Filling cystometry diagnoses DO (involuntary contractions during filling). |
High Yield Summary
-
Continence
- requires: intact pelvic floor + intrinsic urethral mechanism + normal CNS/spinal cord control.
-
Stress UI
- = leakage with ↑abdominal pressure (sphincter weakness); Urge UI = leakage with urgency (detrusor overactivity); Overflow = dribbling with distended bladder (obstruction or hypotonic detrusor); Functional = inability to reach toilet.
-
DIAPERS
- mnemonic for reversible causes — always screen for these before labelling permanent incontinence.
-
Drug causes
- Diuretics/caffeine/alcohol
-
First-line Ix
- MSU C/ST (rule out UTI) + voiding diary. UDS = gold standard but for complex/pre-surgical cases only.
-
OAB treatment ladder
- Conservative (lifestyle, bladder training, PFMT)
-
Antimuscarinics
- Act on M3; S/E = dry mouth, constipation, blurred vision, cognitive impairment. 3–4 weeks to work. Try ≥ 2 before declaring failure.
-
Mirabegron
- β₃-agonist, relaxes detrusor via cAMP pathway. Watch for hypertension.
-
TVT/MUS
- Gold standard surgery for female SUI (> 90% cure at 10 years). For ISD
-
Oral oestrogen worsens UI; vaginal oestrogen improves UUI.
Active Recall - Lecture Notes
[1] Lecture slides: GC 209. Urinary incontinence and overactive bladder.pdf [2] Senior notes: Ryan Ho Urogenital.pdf (Section 8.1 Approach to Urinary Incontinence) [3] Lecture slides: GC 116. I felt a lump below urinary incontinence in females; genital prolapse.pdf (p53) [4] Lecture slides: Block C - I felt a lump below_ urinary incontinence in females; genital prolapse.pdf [5] Senior notes: Maksim Surgery Notes.pdf (pp309, 316, 318) [6] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf (pp829, 831, 834) [7] Senior notes: Ryan Ho Neurology.pdf (p53) [8] Senior notes: Ryan Ho Endocrine.pdf (p98) [9] Senior notes: Adrian Lui Pediatrics Notes.pdf (p338); MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (pp446-447) [15] Senior notes: Ryan Ho Fundamentals.pdf (pp354-355)
GC208 Unconscious After An Accident Head Injury
Unconsciousness following traumatic head injury is a state of impaired awareness resulting from brain damage due to external force, often involving concussion, intracranial hemorrhage, or diffuse axonal injury requiring urgent neurological assessment and management.
GC210 Urinary Tract Infection
A urinary tract infection is an infection of any part of the urinary system—including the urethra, bladder, ureters, or kidneys—most commonly caused by gram-negative bacteria such as *Escherichia coli*, presenting with dysuria, frequency, urgency, and sometimes systemic signs.